Sodium imbalance

hyponatremia and hypernatremia

1. SODIUM IMBALANCE By: Ram Gopal Maurya

2. SODIUM REGULATION Normal value: 135-145mEq/L. 85-90% sodium is extracellular. Sodium is responsible for more than 90%of total osmolality of ECF. Major function is to maintain ECF volume and therefore maintain blood pressure. Daily requirement is about 100mEq or 6gm of sodium chloride. Excess salt is excreted chiefly by kidneys. Total body sodium is mainly regulated by aldosterone and ANP . ADH , which is secreted in response to increased osmolality or decreased blood pressure, primarily regulates [Na + ]

3. HYPONATREMIA Plasma Na+ concentration <135 mM The concentration of sodium in ECF is a reflection of the tonicity of body fluids, not of total body sodium content. Hyponatremia can be associated with low, normal or high tonicity. Hyponatremia -Most common abnormality 15-30% of hospitalized pnts . Basically a water imbalance.

4. Development of Hyponatremia Hyponatremia is a condition of water excess relative to Na+. A defect in renal water excretion in the presence of normal water intake is a prerequisite for the development of hyponatremia . This defect in water excretion is due to high circulating levels of antidiuretic hormone (ADH). With retention of water, hyponatremic patients are unable to lower their urine osmolality < 100 mOsm /kg H2O with the exception of those with psychogenic polydipsia and reset osmostat .

5. Approach to the Patient with Hyponatremia Step 1: Measure Serum Osmolality . plasma osmolality normal low high 280-295 <280 >295 isosmolality hyposmolality hyperosmolality Hyperproteinemia Hyperglycemia Mannitol , Glycerol, Glycine Hyperlipidemia

6. Step 2. Estimate volume status volume status Hypovolemic hypervolemic normovolemic Renal causes Extrarenal causes Diuretics vomiting diarrhoea Mineralocorticoid deficiency Salt-losing nephropathy Cerebral salt wasting

7. Hypervolemic hyponatremia CHF Cirrhosis Nephrotic syndrome AKI & CKD Normovolemiv hyponatremia Psychogenic polydipsia Hypothyroidism Glucocorticoid deficiency Hypokalemia Drugs: NSIAD SIADH

8. Step 3: get urinary sodium and osmolality done Hypovolemic hyponatremia UNa >20 mEq /L RENAL SODIUM LOSS UNa <20 mEq /L EXTRARENAL SODIUM LOSS Hypervolemic hypernatremia UNa >20 mEq /L RENAL FAILURE UNa <20 mEq /L CHF OR CHIRROSIS Normovolemic hyponatremia Uosm > 100 mosm /kg H2O EXCESS OF WATER INTAKE Uosm < 100 mosm /kg H2O EXCESS WATER RETENTION

9. Syndrome Of Inappropriate ADH (SIADH ) A defect in osmoregulation causes vasopressin to be inappropriately stimulated, leading to urinary concentration. MCC of euvolumic hyponatremia Excess vasopressin: CNS disturbances such as hemorrhage, tumors, infections, and trauma. Ectopic vasopressin: Small cell lung cancers, cancer of the duodenum and pancreas, and olfactory neuroblastoma . Idiopathic: seen in elderly(10%).

10. Diagnostic Criteria for SIADH plasma sodium concentration <135 mmol /l. plasma osmolality <280 mOsmol /kg. urine osmolality > 100 mOsmol /kg. urinary sodium concentration >20mEq/L. patient clinically euvolaemic . absence of clinical or biochemical features of adrenal and thyroid dysfunction.

11. Supporting diagnostic criteria for SIADH Serum uric acid <4 mg/Dl. Blood urea nitrogen <10 mg/ dL . Fractional sodium excretion >1%; fractional urea excretion >55%. Failure to improve or worsening of hyponatremia after 0.9% saline infusion. Improvement of hyponatremia with fluid restriction

12. Cerebral salt wasting Is a syndrome described following SAH, head injury, or neurosurgical procedures, as well in other settings. Primary defect is salt wasting from the kidneys with subsequent volume contraction, which stimulates vasopressin release.

13. parameter CSW SIADH HYPOTONIA yes Yes VOLUME STATUS Low Normal to high CVP Low normal HEMATOCRIT High Normal BUN High low URINE Na High High Urine osmolality High High Urine volume High Low Plasma ADH Normal to high High Brain natriuretic peptide Normal to high normal treatment Salt, fludrocortisone Water restriction, 3 % saline, loop diuretics, demeclocycline , urea, vaptans

14. Mineralocorticoid deficiency Hyperkalemia Hyponatremia hypotensive and/or hypovolemic patient with high urine Na+ concentration (much >20 mM )

15. Clinical diagnosis The symptoms primarily neurologic Development of cerebral edema within a rigid skull. headache, lethargy, confusion, gait disorder, nausea, vomiting . In severe hyponatremia as seizures, coma, brain-stem herniation , permanent brain damage or death. Hypo- natremia Mild <135 moderate <130 sever <120

16. Treatment of Hyponatremia as acute (< 48 h duration) or chronic (> 48 h duration) Treatment of Acute Symptomatic Hyponatremia medical emergency. 3 % NaCl is the fluid of choice, because it has high osmolality than most of the patients’ urine osmolality . Raise serum Na+ 1–2 mEq /h for 3 h to 6 hrs from baseline and maximum total 8-12 meq /l/day.

17. amount of Na+ required to achieve the desired level: Amount of Na needed = total body water * desired Na – actual Na . 1 L of 3 % NaCl contains 513 mEq of Na+ One liter of NS contains: 154 mmol /L of Na+

18. Equations : help calculate the initial rate of fluids to be administered. A widely used formula is the Adrogue-Madias formula. Change in serum Na+ with infusing solution= infusate (Na + K)]-serum Na = [Na+] change by 1 liter of infusate . (total body water +1)

19. Treatment of Chronic Symptomatic Hyponatremia For chronic hyponatremia , the plasma [Na] should not rise faster than 0.5 mEq /L per hour i.e. 10–12 mEq /L in 24 hours, and < 18 mEq in 48 hrs. Use 3 % NaCl , but Once symptoms and signs improve, either water restriction or normal saline should be started

20. Treatment of Asymptomatic Hyponatremia In such patients, check volume status. For hypovolemic patients , administration of normal saline will improve both hemodynamics and serum [Na+]. FLUID EXCESS IS PRESENT.

21. Fluid restriction required : the sum of urine [Na+] and [K+] divided by serum [Na+] can be used in the restriction of fluids/day. Ratio Daily fluid intake ( mL ) >1 <500 1 500 to 700 < 1 1000 simplest way to restrict fluids: input = output

22. Specific tratment SIADH: Treat the underlying cause of SIADH Restrict fluid. DIURETICS : Furosemide (40 mg) can be tried with high Na+ intake. Demeclocycline at 300– 600 mg twice daily induces nephrogenic diabetes insipidus . major problem with demeclocycline is nephrotoxicity . Osmotic diuresis V2 receptor antagonists ( vaptans ) can be used to suppress ADH action.

23. Osmotic Demyelination Syndrome Previously called central pontine myelinolysis , is a complication of treatment of hyponatremia . Due to rapid correction of chronic hyponatremia . When serum [Na+] is rapidly raised, the plasma osmolality becomes hypertonic to the brain with resultant water movement from the brain. This cerebral dehydration probably causes myelinolysis and ODS.

24. Several risk factors for precipitation of OSD have been identified. These are: 1. Chronic 2. Serum [Na+] < 105 mEq /L 3. Chronic alcoholism 4. Malnutrition 5. Hypokalemia 6. Severe liver disease 7. Elderly women on thiazide diuretics

25. Clinical Manifestations 1. Paraparesis or quadriparesis 2. Pseudobulbar symptoms ( dysarthria or dysphagia ) 3. Locked-in syndrome (preserved intellectual capacity without expression), 4. Movement or behavioral disorders Management is supportive. Early reports showed 100 % mortality.

26. HYPERNATREMIA Hypernatremia is defined as serum or plasma [Na+] > 145 mEq /L Hypernatremia is seen in about 1% of hospitalized patients and is more common (7%) in intensive care unit patients.

27. Etiology Hypernatremia may be caused by a primary Na gain or a water deficit , the latter being much more common. Normally, this hyperosmolar state stimulates thirst and the excretion of a maximally concentrated urine. For hypernatremia to persist, one or both of these compensatory mechanisms must also be impaired .

28. Patients at Risk for Hypernatremia 1.Elderly 2. Children 3. Diabetics with uncontrolled glucose 4. Patients with polyuria 5. Hospitalized patients Lack of adequate free water intake or administration. Impaired water conservation due to concentrating inability Lactulose administration Osmotic diuretics ( mannitol ) Normal or hypertonic saline administration Tube feedings Mechanical ventilation

29. Approach

30. Step 1: Estimate Volume Status HYPO; NORMO; HYPER Step 2: measure 1. Plasma and urine osmolalities 2. Urine Na+ and K+

31. Signs and Symptoms of Hypernatremia Mostly neurologic due to brain shrinkage and tearing of cerebral vessels . Acute hypernatremia : nausea, vomiting, lethargy, irritability, and weakness. These signs and symptoms may progress to seizures and coma. Chronic hypernatremia (present for > 1–2 days): less neurologic signs and symptoms because of brain adaptation; however, weakness, nystagmus , and depressed sensorium may be seen.

32. Specific Causes of Hypernatremia Central Diabetes insipidus (DI) Central DI is due to failure to synthesize or release ADH from hypothalamus. Two types of central DI: complete and partial Thirst mechanism is intact in most except in patients with craniopharyngiomas (post-operative) Urine osmolality is usually ≤ 100 mOsm /kg H2O in complete form Distal nephron responds to ADH action. nocturia is common . Post-traumatic, post-surgical, metastatic tumors, granulomas , and CNS infections are the most common causes of acquired central DI.

33. Nephrogenic DI Tubular resistance to ADH action despite adequate circulating levels of ADH. Thirst mechanism is intact Urine osmolality is < 300 mOsm /kg H2O Causes are both congenital and acquired Acquired nephrogenic DI: Important causes include CKD, hypokalemia , hypercalcemia , protein malnutrition, sickle cell disease, and lithium, or demeclocycline treatment .

34. Gestational DI Occurs during late pregnancy and resolves after delivery. Caused by degradation of vasopressin (ADH) by the enzyme vasopressinase , and this enzyme is produced by the placenta Treatment is desmopressin ( dDAVP ), which is not degraded by vasopressinase .

35. APPORACH TO POLUURIA

36. TREATMENT OF HYPOVOLEMIC HYPERNATREMIA Management is aimed at the two consequences of hypotonic fluid loss: (a) loss of sodium, (b) loss of water in excess of sodium (the free water deficit). Volume Resuscitation: any signs of a low flow state (e.g., cold extremities, a decrease in blood pressure or urine output) should prompt immediate volume resuscitation with isotonic saline.

37. Free Water Replacement: The calculation of free water deficit Current TBW = Normal TBW × (140/Current [ PNa ]) H2O Deficit (L) = Normal TBW – Current TBW = TBW ( 1 – 140/ Current NA)

38. REPLACEMENT VOLUME: Free water deficits are corrected with sodium-containing fluids such as 0.45% NaCL Volume (L) = H2O Deficit × (140/[Na] in IV Fluid)

39. RATE OF REPLA CEMENT: aggressive replacement of free water deficits can produce cell swelling and cerebral edema. the decrease in plasma [Na+] should not exceed 0.5 mEq /L per hour during free water replacement time needed to reduce the plasma [Na+] to 140 mEq /L at a rate of 0.5 mEq /L/hr is Actual Na – 140 0.5

40. Treatment of normovolemic hypernatremia Diabetes Insipidus : The hallmark of DI is a dilute urine in the face of hypertonic plasma.

41. CENTAL DI dDAVP is the drug of choice for central DI Available as nasal spray or oral form Use the lowest dose 5–10 µg nasally or 0.1 or 0.2 mg orally at bedtime to avoid nocturia and hyponatremia . VASOPRESSIN: dose is 2 to 5 Units of aqueous vasopressin given subcutaneously every 4 to 6 hours

42. NEPHROGENIC DI Congenital DI patients should receive enough water to prevent dehydration. Thiazide diuretics may be helpful. Removal of the cause

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